BIOL 340 Mammalian Physiology Lecture 12

The Heart
Midterm 2

Part 2
Cardiac Physiology
 Sequence of atrial and ventricular contractions
• 4-chambered heart (2 atria, 2 ventricles, left and
right completely separated in mammals & birds), from to
unidirectional blood flow regulated by valves body to lung
• Blood returns from the body through inferior and body
superior vena cava into right atrium from
lung
• Enters right ventricle under control of tricuspid
valve
• Enters pulmonary trunk ( pulmonary arteries)
under control of pulmonary semilunar valve R L Exaggerated for
illustration
purposes!
• Returns from lung through 4 pulmonary veins into All chambers are
left atrium always filled
• Enters left ventricle under control of mitral with blood:
there is no air!
(bicuspid) valve
• Enters Aorta under control of aortic semilunar
valvea  systemic arteries from to
body body
Sequence of atrial and ventricular contractions
This highly coordinated from to
sequence of atrial and body to lung
ventricular contractions arises body
from
from a highly coordinated lung
spread of electrical excitation
of cardiac muscle cells
R L

from to
body body
Electrical excitation of the heart: basics
• In vertebrates, heart muscle contractions are myogenic
(intrinsic pacemaker cells in the heart).
• Heart contracts as a unit. Heart muscles are a functional
syncytium. Electrical excitation spreads through gap
junctions and specialized non-contractile cells, does not
require chemical transmitters.
• CNS only has modulatory function (autonomic nervous
system).
• Very long refractory period  no summation / no tetanus
contraction
 Sequence of excitation
Intrinsic cardiac conduction system
• Non-contractile cardiac cells specialized
to initiate and distribute impulses
• Ensures depolarization and contraction
in orderly, sequential manner

R L
 Sequence of excitation
Pacemaker – pacemaker potential ()
• ~1% of cardiac fibers are autorhythmic (SA & AV nodes, rest of
Sinoatrial (SA) node
the conduction system to some degree)
• Unstable resting membrane potential, continuously
depolarizing
• Pacemaker potential is driven by slow Na + channels after
action potential (K+ channels closed)

Atrioventricular (AV) node

R L
 Sequence of excitation
Pacemaker – action potential ()
• When threshold is reached (~-40 mV), action potential is
Sinoatrial (SA) node
initiated.
• Action potential is driven by voltage-gated Ca2+ channels
rather than Na+ channels (much longer than usual
neuronal or skeletal muscle fiber action potentials)

Atrioventricular (AV) node

R L
 Sequence of excitation
Pacemaker – repolarization ()
• Repolarization occurs because voltage-gated Ca2+
Sinoatrial (SA) node
channels inactivate and K+ channels open
• K+ channels close after repolarization, initiating next
pacemaker potential

Atrioventricular (AV) node

R L
 Sequence of excitation
Sinoatrial (SA) node
Sinoatrial (SA) node
• In right atrial wall
• The true pacemaker (fastest depolarization
rate), resetting other autorhythmic cells
• Generates the regular sinus rhythm (75
impulses per minute)
• Without SA input, AV node can take over (50
impulses per minute) or rest of autorhythmic
fibers (30 impulses per minute)

R L
 Sequence of excitation
Atrioventricular (AV) node
R L
Atrioventricular (AV) node
• In inferior portion of interatrial septum
• Reset by impulses traveling through gap
junctions from SA node (~50 impulses per
minute without SA input)
• Smaller fibers, fewer gap junctions  slows
conduction (~100 ms delay)
• Delay is important to separate atrial from
ventricular contractions
 Sequence of excitation
AV bundle (bundle of His)
• Atria and ventricles NOT directly connected by
gap junctions
• All excitation of ventricles arrives through the
AV bundle
• Splits into right and left pathway towards the
ventricular apex
AV bundle
(bundle of His)

R L
 Sequence of excitation
Subendocardial conducting network
(Purkinje fibers)
• Rapid conduction from apex through the
ventricles
• Left side more elaborate because left ventricle
walls are much larger
• Ventricle cell excitation spreads through
abundant gap junctions
Subendocardial conducting network
(Purkinje fibers)

R L
 Sequence of excitation
Total pattern from SA impulses to
ventricular contraction is fixed
(220 ms)
 Changes in heart rate mean the
frequency with which this pattern
is repeated changes, not the
pattern itself!

R L FAST SLOW
 Action potentials in contractile cardiac muscle cells

Pacemaker and action potentials in

pacemaker cells
 Action potentials in contractile cardiac muscle cells
 Depolarization
• Fast voltage-gated Na+ channels
open (positive feedback loop)

 Plateau phase
• Slow Ca2+ channels open (K+
channels closed)

 Repolarization
• Slow Ca2+ channels inactivating, K+
channels opening

Contraction
• over after 300 ms (no summation!)
Temporal structure and waveforms
Temporal structure and waveforms
Atrial excitation

Ventricular excitation
Temporal structure and waveforms
Atrial excitation

Ventricular excitation
Electrocardiograms (EKG, ECG)
Electrocardiograms (EKG, ECG)
• Electrical activity of the
heart can be
extracellularly recorded
throughout the body
• Even simple electrode
arrangements yield
typical waveforms from
the whole heart
Einthoven’s triangle
ECG: temporal structure and waveforms
Electrocardiograms (EKG, ECG)
• ECGs are extracellular recordings,
they detect the sum of membrane
potential changes from many cells.
• Only CHANGES are detected:
• depolarizations or
hyperpolarizations cause
negative or positive deflections in
the ECG while the membrane
potentials change.
• Stable membrane potentials are
not detected, no matter if the
cells are at rest or not.
Electrocardiograms (EKG, ECG)
Electrocardiograms (EKG, ECG)

r
 Normal and abnormal ECGs

R
R
P T T

P P P P P P P
Cardiac Cycle
Cardiac Cycle
 Cardiac Output

Cardiac output (CO): Volume of blood pumped by each ventricle in

one minute
CO = heart rate (HR) x stroke volume (SV)
• HR = number of beats per minute
• SV = volume of blood pumped out by a ventricle with each beat
 Cardiac Output

Regulation of stroke volume: SV = EDV – ESV

• EDV (end diastolic volume): blood volume that collects in ventricle
during diastole
• ESV (end systolic volume): blood volume remaining in ventricle
after contraction
 Cardiac Output

Regulation of stroke volume: SV = EDV – ESV

• Preload: how much heart muscle is stretched before ventricular contraction,
venous return
• Contractility: how much muscle cells can contract, mostly dependent on Ca2+
• Afterload: pressure ventricles must overcome against aortic back pressure
(relatively constant, unless patient with hypertension)
 Cardiac Output
Regulation by cardiovascular center in the medulla
• Cardioacceleratory center:  sympathetic output (norepinephrine) to heart (direct
and through adrenal medulla)  heart rate and force
• Cardioinhibitory center:  parasympathetic output (ACh) to heart   heart rate
Cardiac Output
Cardiac Output
Cardiac Output
 Summary
• The highly coordinated sequence of atrial and ventricular contractions arises from a
highly coordinated spread of electrical excitation of cardiac muscle cells.
• Heart muscle contractions are myogenic, evoked by intrinsic pacemaker cells (no
chemical transmission for excitation).
• The sinoatrial (SA) node usually sets the pace of heart beats, resetting the slower
atrioventricular (AV) node, and the rest of the conduction system.
• Pacemaker potentials are driven by slow sodium currents, action potentials are long-
lasting (driven by calcium currents or sodium and calcium currents).
• Excitation is transmitted through gap junctions, separated between atria and ventricles:
The SA node excites the atria and the AV node. The AV node is the sole connection
between atria and ventricles. The AV node causes some delay and then excitation travels
through the conduction system to the apex, and from there spreads up the ventricles
through Purkinje fibers and gap junctions between ventricular cells.
 Summary
• The electrical activity of the heart can be measured from the entire body extracellularly
with ECG electrodes (important diagnostic tool). The different sequential waves of the
ECG correspond to the path of excitation from atria to ventricles.
• The cardiac cycle of alternating diastoles and systoles is associated with blood volume
and pressure changes that control the operation of the valves and ensure unidirectional
flow.
• Cardiac output depends on heart rate and stroke volume, both of which are controlled by
the brain stem through sympathetic and parasympathetic output to the pacemakers
(both) and ventricles (sympathetic only).
REVIEW QUESTIONS • Why does it make sense that the heart action potentials have
a large calcium component?
• What is very different about the temporal relationship of
excitation and contraction in heart vs skeletal muscle?
• What is the special role of the AV node?
• How is cardiac output autonomic control coordinated with
control of total peripheral resistance?
• The last figure/diagram only shows which factors contribute
to increase of cardiac output. What would the version of this
figure look like for decrease of cardiac output?